Abstract
Objective: In hypertensive patients, the activation of the renin-angiotensin-aldosterone system is associated with an increase of subclinical vascular and cardiac damage. Our study aimed to compare some early markers of cardiovascular organ damage between patients with essential hypertension and patients with secondary hypertension, in particular primary aldosteronism. Design and method: Fifty-seven hypertensive patients (mean age: 44,4±13,6 years, 60.7% males) were included, 47 with essential hypertension and 10 with primary hyperaldosteronism. Peripheral blood pressure (pBP), central blood pressure (cBP) and pulse wave velocity (PWV) were assessed by the SphygmoCorXCEL. The carotid Intima-Media Thickness (cIMT) and the carotid Distensibility Coefficient (cCD) were measured by a scanner connected with an image acquisition and analysis system (CardiovascularSuite). Left ventricular mass index (LVMI) and relative wall thickness (RWT) were evaluated by transthoracic echocardiography. Results: Patients with primary aldosteronism have higher cIMT and PWV values compared to patients with essential hypertension (0.7±0.1mm vs. 0.6±0.1 mm, p = 0.02 and 8.6±2.5 m/s vs. 7.2±1.5 m/s, p = 0.02; respectively). By linear regression, age was the only variable independently associated with cIMT. On the other hand, various factors such as age, the diagnosis of primary aldosteronism, pSBP and cSBP were independently associated with PWV. Although not statistically significant, LVMI and RWT tended to be higher in the group with primary aldosteronism in comparison to patients with essential hypertension (14.3% vs. 0% exhibited concentric hypertrophy and 42.8% vs. 28.1% showed findings consistent with concentric cardiac remodelling). No differences were found in cDC values between the two groups. Conclusions: The results of this study confirm a possible deleterious impact of aldosteronism on cardiovascular damage in hypertensive patients, more evident for PWV than for cIMT or DC. This fact could suggest a possible different effect of the abnormal hormone secretion at different vascular districts.
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